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. Author manuscript; available in PMC: 2021 Mar 19.
Published in final edited form as: Cell Rep. 2019 Aug 20;28(8):2140–2155.e6. doi: 10.1016/j.celrep.2019.07.059

Figure 7. Tumor Escape Variants Fail to Express MHC I because of a Defect in Tap1 following IFNγ.

Figure 7.

(A) IF staining for tumor cells (CK+), PD-L1, and CD8 in KPC2a tumors in control (−) or αPD-L1 (+) at the indicated time points. Tumors were not easily identifiable in the mice that received αPD-L1 at day 14. Scale bar, 50 μM.

(B) Cell surface expression of indicated proteins ± IFNγ treatment in parental KPC2 cells, KPC2a clone prior to implantation (pre-transfer), and two independent KPC2a escape variants. Representative of n = 2 independent experiments.

(C) Fold induction of antigen processing and/or presentation genes following IFNγ treatment in parental KPC2 cells, KPC2a pre-transfer (KPC2a-PT), and four independently re-derived KPC2a escape variants (KPC2a-EV). Data are mean ± SEM.

(D) Gene expression in cell lines from Figure 7C without IFNγ treatment normalized to housekeeping gene ATP5b. Note that a higher the delta Ct indicates lower target gene expression relative to ATP5b. All qPCR data were performed in triplicate.